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Letter to the Editor

A gene expression profile associated with relapse of cytogenetically normal acute myeloid leukemia is enriched for leukemia stem cell genes

, , , , , , , & show all
Pages 1126-1128 | Received 24 Jan 2014, Accepted 06 Jul 2014, Published online: 18 Aug 2014

Figures & data

Figure 1. Genes differentially expressed between diagnosis and relapse of CN AML. Log2 fold changes compared to the mean of all samples are displayed for the 30 most up- and the 30 most down-regulated genes (i.e. significantly differentially expressed genes with the highest positive and negative mean log2 fold changes between the two disease states). Red, gene expression above the mean; blue, gene expression below the mean. DG, diagnosis; R, relapse.

Figure 1. Genes differentially expressed between diagnosis and relapse of CN AML. Log2 fold changes compared to the mean of all samples are displayed for the 30 most up- and the 30 most down-regulated genes (i.e. significantly differentially expressed genes with the highest positive and negative mean log2 fold changes between the two disease states). Red, gene expression above the mean; blue, gene expression below the mean. DG, diagnosis; R, relapse.

Figure 2. Gene signatures associated with LSCs, HSCs and poor therapy response are enriched in the CN AML relapse profile. Lists of genes associated with functionally defined LSCs [Citation7], cell surface marker-defined HSCs [Citation7], poor response to chemotherapy [Citation10–12] or marker-defined LSCs [Citation9] were probed against the relapse-associated gene expression profile, ranked according to each gene's associated t-statistic, using gene set enrichment analysis (GSEA) [Citation8]. The number of genes present in the relapse profile, as well as the total number of genes, is indicated for each signature. NES, normalized enrichment score; FDR, false discovery rate. Similar results were obtained when genes were ranked according to their log2 fold change between the two disease states.

Figure 2. Gene signatures associated with LSCs, HSCs and poor therapy response are enriched in the CN AML relapse profile. Lists of genes associated with functionally defined LSCs [Citation7], cell surface marker-defined HSCs [Citation7], poor response to chemotherapy [Citation10–12] or marker-defined LSCs [Citation9] were probed against the relapse-associated gene expression profile, ranked according to each gene's associated t-statistic, using gene set enrichment analysis (GSEA) [Citation8]. The number of genes present in the relapse profile, as well as the total number of genes, is indicated for each signature. NES, normalized enrichment score; FDR, false discovery rate. Similar results were obtained when genes were ranked according to their log2 fold change between the two disease states.
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